<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hogea A</submitter><funding>Wellcome Trust</funding><funding>Biotechnology and Biological Sciences Research Council</funding><pagination>2103-2123</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7618066</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>599(7)</volume><pubmed_abstract>&lt;h4>Key points&lt;/h4>Rat somatosensory neurons express a junctional protein, junctophilin-4 (JPH4) JPH4 is necessary for the formation of store operated Ca&lt;sup>2+&lt;/sup> entry (SOCE) complex at the junctions between plasma membrane and endoplasmic reticulum in these neurons. Knockdown of JPH4 impairs endoplasmic reticulum Ca&lt;sup>2+&lt;/sup> store refill and junctional Ca&lt;sup>2+&lt;/sup> signalling in sensory neurons. In vivo knockdown of JPH4 in the dorsal root ganglion (DRG) sensory neurons significantly attenuated experimentally induced inflammatory pain in rats. Junctional nanodomain Ca&lt;sup>2+&lt;/sup> signalling maintained by JPH4 is an important contributor to the inflammatory pain mechanisms.&lt;h4>Abstract&lt;/h4>Junctions of endoplasmic reticulum and plasma membrane (ER-PM junctions) form signalling</pubmed_abstract><journal>The Journal of physiology</journal><pubmed_title>Junctophilin-4 facilitates inflammatory signalling at plasma membrane-endoplasmic reticulum junctions in sensory neurons.</pubmed_title><pmcid>PMC7618066</pmcid><funding_grant_id>BB/R003068/1</funding_grant_id><funding_grant_id>BB/R02104X/1</funding_grant_id><funding_grant_id>212302/Z/18/Z</funding_grant_id><funding_grant_id>212302</funding_grant_id><pubmed_authors>Liang C</pubmed_authors><pubmed_authors>Gamper N</pubmed_authors><pubmed_authors>Huang D</pubmed_authors><pubmed_authors>Shah S</pubmed_authors><pubmed_authors>Hogea A</pubmed_authors><pubmed_authors>Jones F</pubmed_authors><pubmed_authors>Du X</pubmed_authors><pubmed_authors>Hao H</pubmed_authors><pubmed_authors>Carver CM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Junctophilin-4 facilitates inflammatory signalling at plasma membrane-endoplasmic reticulum junctions in sensory neurons.</name><description>&lt;h4>Key points&lt;/h4>Rat somatosensory neurons express a junctional protein, junctophilin-4 (JPH4) JPH4 is necessary for the formation of store operated Ca&lt;sup>2+&lt;/sup> entry (SOCE) complex at the junctions between plasma membrane and endoplasmic reticulum in these neurons. Knockdown of JPH4 impairs endoplasmic reticulum Ca&lt;sup>2+&lt;/sup> store refill and junctional Ca&lt;sup>2+&lt;/sup> signalling in sensory neurons. In vivo knockdown of JPH4 in the dorsal root ganglion (DRG) sensory neurons significantly attenuated experimentally induced inflammatory pain in rats. Junctional nanodomain Ca&lt;sup>2+&lt;/sup> signalling maintained by JPH4 is an important contributor to the inflammatory pain mechanisms.&lt;h4>Abstract&lt;/h4>Junctions of endoplasmic reticulum and plasma membrane (ER-PM junctions) form signalling</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Apr</publication><modification>2026-05-18T03:09:20.776Z</modification><creation>2026-05-18T03:07:13.805Z</creation></dates><accession>S-EPMC7618066</accession><cross_references><pubmed>33569781</pubmed><doi>10.1113/JP281331</doi></cross_references></HashMap>